Basics of ECG

Anusha Verghese,Msc
Nursing

http://emergencymedic.blogspot.com

HISTORY
1842- Italian scientist Carlo Matteucci realizes
that electricity is associated with the heart beat
1876- Irish scientist Marey analyzes the electric
pattern of frogs heart
1895 - William Einthoven , credited for the
invention of EKG
1906 - using the string electrometer EKG,
William Einthoven diagnoses some heart
problems

CONTD
1924 - the noble prize for physiology or
medicine is given to William Einthoven for
his work on EKG
1938 -AHA and Cardiac society of great
Britan defined and position of chest leads
1942Goldberger
increased
Wilsons
Unipolar lead voltage by 50% and made
Augmented leads
2005- successful reduction in time of onset
of chest pain and PTCA by wireless
transmission of ECG on his PDA.

MODERN ECG
INSTRUMENT

What is an EKG?
The electrocardiogram (EKG) is a
representation
of the electrical
events of the cardiac cycle.
Each event has a distinctive
waveform
the study of waveform can lead to
greater insight into a patients cardiac
pathophysiology.

With EKGs we can

identify
Arrhythmias
Myocardial ischemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances (i.e.
hyperkalemia, hypokalemia)
Drug toxicity (i.e. digoxin and drugs
which prolong the QT interval)

Depolarization
Contraction of any muscle is associated with
electrical changes called depolarization
These changes can be detected by
electrodes attached to the surface of the
body

Pacemakers of the Heart

SA Node - Dominant pacemaker with
an intrinsic rate of 60 - 100
beats/minute.
AV Node - Back-up pacemaker with
an intrinsic rate of 40 - 60
beats/minute.
Ventricular cells - Back-up pacemaker
with an intrinsic rate of 20 - 45 bpm.

 Standard calibration
25 mm/s
0.1 mV/mm
Electrical impulse
that travels towards
the electrode
produces an upright
(positive)
deflection

Impulse Conduction & the

ECG
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

The PQRST
P wave - Atrial
depolarization

QRS - Ventricular
depolarization
T wave - Ventricular
repolarization

The PR Interval
Atrial depolarization
+
delay in AV junction
(AV node/Bundle of His)

(delay allows time

for the atria to
contract before the
ventricles contract)

NORMAL ECG

The ECG Paper

Horizontally
One small box - 0.04 s
One large box - 0.20 s

Vertically
One large box - 0.5 mV

EKG Leads
which measure the difference in
electrical potential between two
points
1. Bipolar Leads: Two different points on the body
2. Unipolar Leads: One point on the body and a virtual
reference point with zero electrical potential, located in
the center of the heart

EKG Leads
The standard EKG has 12
leads:
3 Standard Limb Leads
3 Augmented Limb Leads
6 Precordial Leads

Standard Limb Leads

Standard Limb Leads

Augmented Limb
Leads

All Limb Leads

Precordial Leads

Precordial Leads

Right Sided & Posterior

Chest Leads

Arrangement of Leads on
the EKG

Anatomic Groups

(Septum)

Anatomic Groups

(Anterior Wall)

Anatomic Groups

(Lateral Wall)

Anatomic Groups

(Inferior Wall)

Anatomic Groups

(Summary)

ECG RULES
Professor Chamberlains 10 rules of
normal:-

RULE 1

PR interval should be 120 to 200

milliseconds or 3 to 5 little squares

RULE 2

The width of the QRS complex should not

exceed 110 ms, less than 3 little squares

RULE 3

The QRS complex should be dominantly upright

in leads I and II

RULE 4

QRS and T waves tend to have the same

general direction in the limb leads

RULE 5

All waves are negative in lead aVR

RULE 6

The R wave must grow from V1 to at

least V4
The S wave must grow from V1 to at

RULE 7

The ST segment should start isoelectric

except in V1 and V2 where it may be elevated

RULE 8

The P waves should be upright in I, II, and V2 to

V6

RULE 9

There should be no Q wave or only a small q

less than 0.04 seconds in width in I, II, V2 to
V6

RULE 10

The T wave must be upright in I, II, V2 to V6

P wave

Always positive in lead I and II

Always negative in lead aVR
< 3 small squares in duration
< 2.5 small squares in
amplitude
Commonly biphasic in lead V1
Best seen in leads II

Right Atrial Enlargement

Tall (> 2.5 mm), pointed P waves (P Pulmonale)

Left Atrial Enlargement

Notched/bifid (M shaped) P
wave (P mitrale) in limb leads

P
Pulmonal
e
P
Mitrale

Short PR Interval
WPW (WolffParkinson-White)
Syndrome
Accessory
pathway (Bundle
of Kent) allows
early activation
of the ventricle
(delta wave and
short PR interval)

Long PR Interval
First degree Heart Block

QRS Complexes
Nonpathological Q waves may present in I, III,
aVL, V5, and V6
R wave in lead V6 is smaller than V5
Depth of the S wave, should not exceed 30 mm
Pathological Q wave > 2mm deep and > 1mm
wide or > 25% amplitude of the subsequent R
wave

QRS in LVH & RVH

Conditions with Tall R in

V1

Right Atrial and Ventricular

Hypertrophy

Left Ventricular
Hypertrophy

Sokolow & Lyon Criteria

S in V1+ R in V5 or V6 > 35 mm
An R wave of 11 to 13 mm (1.1 to
1.3 mV) or more in lead aVL is
another sign of LVH

ST Segment
ST Segment is flat (isoelectric)
Elevation or depression of ST
segment by 1 mm or more
J (Junction) point is the point
between QRS and ST segment

Variable Shapes Of ST
Segment Elevations in AMI

Goldberger AL. Goldberger: Clinical Electrocardiography: A

Simplified Approach. 7th ed: Mosby Elsevier; 2006.

T wave
Normal T wave is asymmetrical, first half
having a gradual slope than the second
Should be at least 1/8 but less than 2/3 of the
amplitude of the R
T wave amplitude rarely exceeds 10 mm
Abnormal T waves are symmetrical, tall,
peaked, biphasic or inverted.
T wave follows the direction of the QRS
deflection.

T wave

QT interval
1. Total duration of Depolarization and
Repolarization
2. QT interval decreases when heart
rate increases
3. For HR = 70 bpm, QT<0.40 sec.
4. QT interval should be 0.35 0.45 s,
5. Should not be more than half of the
interval between adjacent R waves (R
R interval).

QT Interval

U wave
U wave related to afterdepolarizations
which follow repolarization
U waves are small, round, symmetrical
and positive in lead II, with amplitude < 2
mm
U wave direction is the same as T wave
More prominent at slow heart rates

Determining the
Heart Rate
Rule of 300/1500
10 Second Rule

Rule of 300
Count the number of big boxes
between two QRS complexes, and
divide this into 300. (smaller boxes
with 1500)
for regular rhythms.

What is the heart

rate?

(300 / 6) = 50 bpm

What is the heart

rate?

(300 / ~ 4) = ~ 75 bpm

What is the heart

rate?

(300 / 1.5) = 200 bpm

The Rule of 300

It may be easiest to memorize the following
table:
No of big
boxes

Rate

300

150

100

75

60

50

10 Second
Rule
EKGs record 10 seconds of rhythm per
page,
Count the number of beats present on the
EKG
Multiply by 6
For irregular rhythms.

What is the heart

rate?

33 x 6 = 198 bpm

Calculation of Heart Rate

Question
Calculate the heart rate

The QRS Axis

The QRS axis represents overall
direction of the hearts electrical
activity.
Abnormalities hint at:
Ventricular enlargement
Conduction blocks (i.e.
hemiblocks)

The QRS Axis

Normal QRS axis from -30 to
+90.

-30 to -90 is referred to as a

left axis deviation (LAD)

+90 to +180 is referred to as

a right axis deviation (RAD)

Determining the Axis

The Quadrant Approach
The Equiphasic Approach

Determining the Axis

Predominantly
Positive

Predominantly
Negative

Equiphasic

1.
2.
3.

The Quadrant
QRS complex in leads I andApproach
aVF
determine if they are predominantly positive or
negative.
The combination should place the axis into one of
the 4 quadrants below.

The Quadrant
Approach
When LAD is present,
If the QRS in II is positive, the LAD is nonpathologic or the axis is normal
If negative, it is pathologic.

Quadrant Approach:
Example 1

Negative in I, positive in aVF RAD

Quadrant Approach:
Example 2

Positive in I, negative in aVF

Predominantly positive in II

Normal Axis (non-pathologic LAD)

The Equiphasic
Approach
1. Most equiphasic QRS complex.
2. Identified Lead lies 90 away from the lead
3. QRS in this second lead is positive or
Negative

QRS Axis = -30 degrees

QRS Axis = +90 degrees-KH

Equiphasic Approach

Equiphasic in aVF Predominantly positive in I QRS axis 0

BRADYARRYTHMI
A

Classification
Sinus Bradycardia
Junctional Rhythm
Sino Atrial Block
Atrioventricular block

Impulse Conduction & the

ECG
Sinoatrial node
AV node
Bundle of His
Bundle Branches

Sinus Bradycardia

Junctional Rhythm

SA Block
Sinus impulses is blocked within the SA
junction
Between SA node and surrounding
myocardium
Abscent of complete Cardiac cycle
Occures irregularly and unpredictably
Present :Young athletes, Digitalis,
Hypokalemia, Sick Sinus Syndrome

AV Block
First Degree AV Block
Second Degree AV Block
Third Degree AV Block

First Degree AV Block

Delay in the conduction through the conducting
system
Prolong P-R interval
All P waves are followed by QRS
Associated with : AC Rheumati Carditis, Digitalis, Beta
Blocker, excessive vagal tone, ischemia, intrinsic
disease in the AV junction or bundle branch system.

Second Degree AV Block

Intermittent failure of AV conduction
Impulse blocked by AV node
Types:
Mobitz type 1 (Wenckebach
Phenomenon)
Mobitz type 2

Mobitz type 1 (Wenckebach Phenomenon)

The 3 rules of "classic AV Wenckebach"

1. Decreasing RR intervals until pause;
2. Pause is less than preceding 2 RR intervals
3. RR interval after the pause is greater than RR prior to
pause.

Mobitz type 1 (Wenckebach

Phenomenon)

Mobitz type 2

Usually a sign of bilateral bundle branch disease.

One of the branches should be completely blocked;
most likely blocked in the right bundle
P waves may blocked somewhere in the AV junction, the
His bundle.

Third Degree Heart Block

CHB evidenced by the AV dissociation

A junctional escape rhythm at 45 bpm.
The PP intervals vary because of ventriculophasic sinus arrhythmia;

Third Degree Heart Block

3rd degree AV block with a left ventricular escape rhythm,

'B' the right ventricular pacemaker rhythm is shown.

AV
Dissociation

The nonconducted PAC's set up a long pause which

is terminated by ventricular escapes;
Wider QRS morphology of the escape beats
indicating their ventricular origin.

AV
Dissociation

Due to Accelerated ventricular rhythm

Putting it all Together

Do you think this person is having
a myocardial infarction. If so,
where?

Interpretation
Yes, this person is having an acute
anterior wall myocardial
infarction.

Putting it all Together

Now, where do you think this
person is having a myocardial
infarction?

Inferior Wall MI
This is an inferior MI. Note the ST
elevation in leads II, III and aVF.

Putting it all Together

How about now?

Anterolateral MI
This persons MI involves both the
anterior wall (V2-V4) and the lateral
wall (V5-V6, I, and aVL)!

Rhythm #6

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

70 bpm
regular
flutter waves
none
0.06 s

Interpretation? Atrial Flutter

Rhythm #7

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

74 148 bpm
Regular
regular
Normal none
0.16 s none
0.08 s

Interpretation? Paroxysmal Supraventricular

Tachycardia (PSVT)

PSVT

Deviation from NSR

The heart rate suddenly speeds
up, often triggered by a PAC (not
seen here) and the P waves are
lost.

Ventricular Arrhythmias
Ventricular Tachycardia
Ventricular Fibrillation

Rhythm #8

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

160 bpm
regular
none
none
wide (> 0.12 sec)

Interpretation? Ventricular Tachycardia

Ventricular Tachycardia

Deviation from NSR

Impulse is originating in the
ventricles (no P waves, wide
QRS).

Rhythm #9

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

none
irregularly irreg.
none
none
wide, if recognizable

Interpretation? Ventricular Fibrillation

Ventricular Fibrillation

Deviation from NSR

Completely abnormal.

Arrhythmia Formation
Arrhythmias can arise from
problems in the:
Sinus node
Atrial cells
AV junction
Ventricular cells

SA Node Problems
The SA Node
can:
fire too slow
fire too fast

Sinus Bradycardia
Sinus Tachycardia

Sinus Tachycardia may be an appropriate

response to stress.

Atrial Cell Problems

Atrial cells can:
fire occasionally
from a focus

Premature Atrial
Contractions
fire continuously
(PACs)
due to a looping
re-entrant
circuit

Atrial Flutter

AV Junctional Problems
The AV junction
can:
Paroxysmal
fire continuously
Supraventricula
due to a looping
r Tachycardia
re-entrant circuit
AV Junctional
block impulses
Blocks
coming from the
SA Node

Rhythm #1

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

30 bpm
regular
normal
0.12 s
0.10 s

Interpretation? Sinus Bradycardia

Rhythm #2

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

130 bpm
regular
normal
0.16 s
0.08 s

Interpretation? Sinus Tachycardia

Rhythm #3

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

70 bpm
occasionally irreg.
2/7 different contour
0.14 s (except 2/7)
0.08 s

Interpretation? NSR with Premature Atrial

Contractions

Premature Atrial
Contractions
Deviation from NSR
These ectopic beats originate in
the atria (but not in the SA
node), therefore the contour of
the P wave, the PR interval, and
the timing are different than a
normally generated pulse from
the SA node.

Rhythm #4

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

60 bpm
occasionally irreg.
none for 7th QRS
0.14 s
0.08 s (7th wide)

Interpretation? Sinus Rhythm with 1 PVC

Ventricular Conduction

Normal

Abnormal

Signal moves rapidly

through the ventricles

Signal moves slowly

through the ventricles

AV Nodal Blocks
1st Degree AV Block
2nd Degree AV Block, Type I
2nd Degree AV Block, Type II
3rd Degree AV Block

Rhythm #10

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

60 bpm
regular
normal
0.36 s
0.08 s

Interpretation? 1st Degree AV Block

1st Degree AV Block

Etiology: Prolonged conduction

delay in the AV node or Bundle of
His.

Rhythm #11

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

50 bpm
regularly irregular
nl, but 4th no QRS
lengthens
0.08 s

Interpretation? 2nd Degree AV Block, Type I

Rhythm #12

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

40 bpm
regular
nl, 2 of 3 no QRS
0.14 s
0.08 s

Interpretation? 2nd Degree AV Block, Type II

2nd Degree AV Block, Type

II
Deviation from NSR
Occasional P waves are
completely blocked (P wave not
followed by QRS).

Rhythm #13

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

40 bpm
regular
no relation to QRS
none
wide (> 0.12 s)

Interpretation? 3rd Degree AV Block

3rd Degree AV Block

Deviation from NSR

The P waves are completely
blocked in the AV junction; QRS
complexes originate
independently from below the
junction.

Supraventricular
Arrhythmias
Atrial Fibrillation
Atrial Flutter
Paroxysmal Supraventricular
Tachycardia

Rhythm #5

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

100 bpm
irregularly irregular
none
none
0.06 s

Interpretation? Atrial Fibrillation

Atrial Fibrillation
Deviation from NSR
No organized atrial depolarization,
so no normal P waves (impulses are
not originating from the sinus node).
Atrial activity is chaotic (resulting in
an irregularly irregular rate).
Common, affects 2-4%, up to 5-10%
if > 80 years old

Rhythm #6

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

70 bpm
regular
flutter waves
none
0.06 s

Interpretation? Atrial Flutter

Rhythm #7

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

74 148 bpm
Regular
regular
Normal none
0.16 s none
0.08 s

Interpretation? Paroxysmal Supraventricular

Tachycardia (PSVT)

PSVT

Deviation from NSR

The heart rate suddenly speeds
up, often triggered by a PAC (not
seen here) and the P waves are
lost.

Ventricular Arrhythmias
Ventricular Tachycardia
Ventricular Fibrillation

Rhythm #8

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

160 bpm
regular
none
none
wide (> 0.12 sec)

Interpretation? Ventricular Tachycardia

Ventricular Tachycardia

Deviation from NSR

Impulse is originating in the
ventricles (no P waves, wide
QRS).

Rhythm #9

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

none
irregularly irreg.
none
none
wide, if recognizable

Interpretation? Ventricular Fibrillation

Ventricular Fibrillation

Deviation from NSR

Completely abnormal.

Diagnosing a MI
To diagnose a myocardial infarction
you need to go beyond looking at a
rhythm strip and obtain a 12-Lead
ECG.
12-Lead
ECG

Rhythm
Strip

Views of the Heart

Some leads get
a good view of
the:
Anterior portion
of the heart

Inferior portion
of the heart

Lateral portion
of the heart

ST Elevation
One way to
diagnose an
acute MI is
to look for
elevation of
the ST
segment.

ST Elevation (cont)
Elevation of
the ST segment
(greater than 1
small box) in 2
leads is
consistent with
a myocardial
infarction.

Anterior View of the Heart

The anterior portion of the heart is
best viewed using leads V1- V4.

Anterior Myocardial
Infarction

If you see changes in leads V1 V4 that are consistent with a

myocardial infarction, you can
conclude that it is an anterior
wall myocardial infarction.

Putting it all Together

Do you think this person is having
a myocardial infarction. If so,
where?

Interpretation
Yes, this person is having an acute
anterior wall myocardial
infarction.

Other MI Locations
Now that you know where to look
for an anterior wall myocardial
infarction lets look at how you
would determine if the MI involves
the lateral wall or the inferior wall
of the heart.

Other MI Locations
First, take a look
again at this
picture of the
heart.

Anterior portion
of the heart

Inferior portion
of the heart

Lateral portion
of the heart

Other MI Locations
Second, remember that the 12-leads of the ECG look at
different portions of the heart. The limb and
augmented leads see electrical activity moving
inferiorly (II, III and aVF), to the left (I, aVL) and to the
right (aVR). Whereas, the precordial leads see
electrical activity in the posterior to anterior direction.

Limb Leads

Augmented Leads

Precordial Leads

Other MI Locations
Now, using these 3 diagrams lets figure where to
look for a lateral wall and inferior wall MI.

Limb Leads

Augmented Leads

Precordial Leads

Anterior MI
Remember the anterior portion of the
heart is best viewed using leads V1- V4.
Limb Leads

Augmented Leads

Precordial Leads

Lateral MI
So what leads do you think
the lateral portion of the
heart is best viewed?

Limb Leads

Leads I, aVL, and V5- V6

Augmented Leads

Precordial Leads

Inferior MI
Now how about the
inferior portion of
the heart?

Limb Leads

Leads II, III and aVF

Augmented Leads

Precordial Leads

Putting it all Together

Now, where do you think this
person is having a myocardial
infarction?

Inferior Wall MI
This is an inferior MI. Note the ST
elevation in leads II, III and aVF.

Putting it all Together

How about now?

Anterolateral MI
This persons MI involves both the
anterior wall (V2-V4) and the lateral
wall (V5-V6, I, and aVL)!

RIGHT ATRIAL ENLARGEMENT

Right atrial enlargement

Take a look at this ECG. What do you notice
about the P waves?

The P waves are tall, especially in leads II, III and avF.
Ouch! They would hurt to sit on!!

Right atrial enlargement

To diagnose RAE you can use the following criteria:
II
V1 or V2

P > 2.5 mm, or

P > 1.5 mm

> 1 boxes (in height)

> 2 boxes (in height)

Remember 1 small
box in height = 1 mm

A cause of RAE is RVH from pulmonary hypertension.

Left atrial enlargement

Take a look at this ECG. What do you notice
about the P waves?

Notched

Negative deflection

The P waves in lead II are notched and in lead V1 they

have a deep and wide negative component.

Left atrial enlargement

To diagnose LAE you can use the following criteria:
II
V1

> 0.04 s (1 box) between notched peaks, or

Neg. deflection > 1 box wide x 1 box deep

Normal

LAE

A common cause of LAE is LVH from hypertension.

Left Ventricular
Hypertrophy

Left Ventricular
Hypertrophy
Compare these two 12-lead ECGs. What stands
out as different with the second one?

Normal

Left Ventricular Hypertrophy

Answer: The QRS complexes are very tall

(increased voltage)

Left Ventricular
Hypertrophy
Criteria exists to diagnose LVH using a 12-lead ECG.
For example:
The R wave in V5 or V6 plus the S wave in V1 or V2
exceeds 35 mm.

However, for now, all

you need to know is
that the QRS voltage
increases with LVH.

Right ventricular hypertrophy

Take a look at this ECG. What do you notice
about the axis and QRS complexes over the
right ventricle (V1, V2)?

There is right axis deviation (negative in I, positive in II) and

there are tall R waves in V1, V2.

Right ventricular hypertrophy

To diagnose RVH you can use the following criteria:

V1

Right axis deviation, and

R wave > 7mm tall

A common
cause of RVH
is left heart
failure.

Right ventricular hypertrophy

Compare the R waves in V1, V2 from a normal ECG
and one from a person with RVH.
Notice the R wave is normally small in V1, V2 because
the right ventricle does not have a lot of muscle mass.
But in the hypertrophied right ventricle the R wave is
tall in V1, V2.

Normal

RVH

Left ventricular hypertrophy

Take a look at this ECG. What do you notice
about the axis and QRS complexes over the
left ventricle (V5, V6) and right ventricle (V1,
V2)?
The deep S waves
seen in the leads over
the right ventricle are
created because the
heart is depolarizing
left, superior and
posterior (away from
leads V1, V2).

There is left axis deviation (positive in I, negative in II) and there

are tall R waves in V5, V6 and deep S waves in V1, V2.

Left ventricular hypertrophy

To diagnose LVH you can use the following
criteria*:

R in V5 (or V6) + S in V1 (or V2) > 35

mm, or
avL

R > 13 mm

S = 13 mm

* There are several

other criteria for the
diagnosis of LVH.

R = 25 mm

A common cause of LVH

is hypertension.

Bundle Branch
Blocks

Normal Impulse Conduction

Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

Bundle Branch Blocks

So, conduction in
the Bundle Branches
and Purkinje fibers
are seen as the QRS
complex on the ECG.

Therefore, a conduction
block of the Bundle
Branches would be
reflected as a change in
the QRS complex.

Right
BBB

Bundle Branch Blocks

With Bundle Branch Blocks you will see two
changes on the ECG.
1. QRS complex widens (> 0.12 sec).
2. QRS morphology changes (varies depending on
ECG lead, and if it is a right vs. left bundle
branch block).

Right Bundle Branch Blocks

What QRS morphology is characteristic?

For RBBB the wide QRS complex assumes a

unique, virtually diagnostic shape in those
leads overlying the right ventricle (V1 and V2).
V1

Rabbit Ears

RBBB

Left Bundle Branch Blocks

What QRS morphology is characteristic?

For LBBB the wide QRS complex assumes a

characteristic change in shape in those leads
opposite the left ventricle (right ventricular
leads - V1 and V2).
Normal

Broad,
deep S
waves

HYPERKALEMIA

HYPERKALEMIA

SEVERE HYPERKALEMIA

HYPOKALEMIA

HYPOKALEMIA

HYPOKALEMIA

HYPERCALCEMIA

HYPOCALCEMIA

ACUTE PERICARDITIS

ACUTE PERICARDITIS

CARDIAC TAMPONADE

PERICARDIAL EFFUSIONElectrical alterans

HYPOTHERMIA-OSBORNE
WAVE

HYPOTHERMIAGiant Osborne waves